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LDLC of 8.9 mmol/L. Should I be concerned?



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  • #31
    Originally posted by sharperhawk View Post

    Can you point me to an overview of the theory?
    I think Broda Barnes said it best. You can find at least one of his books, in its entirety, online. That being said, here are some of the highlights:

    In animal experiments, things that affect thyroid hormones affect atherosclerosis.
    Hypothyroidism raises cholesterol, which explains the classic correlation.
    Hypothyroidism also weakens the immune system. In a society without antibiotics, hypothyroid people tend to die of infection before heart disease has a chance to kill them, which explains why heart disease is not a killer in "older" societies. Antibiotics indirectly allow heart disease.
    Diabetes causes hypothyroidism, which explains why diabetes causes heart disease.
    The method of diagnosing hypothyroidism was changed, such that only about 5% of people now qualify, while previously as much as 40% of the population might have been hypothyroid. This explains why heart disease is so much more common than hypothyroidism officially is.
    Broda Barnes essentially eliminated heart disease among his patients by prescribing thyroid hormones.
    My opinions and some justification


    • #32
      If hypothyroidism is linked to CVD, then I wonder how that places into both D3 and K2. One cannot have atherosclerosis if there is no hardening of material in the arterial walls. Calcium is what causes all the junk to harden together, and the reason calcium ends up in the arterial walls is because it's not being deposited in the appropriate places (bones and teeth), and this is something that K2 does. K2 also pulls it from the places it shouldn't be like arteries.

      So I'm curious then, is there a direct correlation between hypothyroidism and a deficiency in K2? It's estimated that most of the population is deficient in K2 (though I'm not sure how researchers assume this considering K2 isn't realistically testable in humans). K2 is also primarily found in fatty foods, and there is no real evidence that K1 (found in plants) converts to K2 in the liver as all tests on that have been done on animals which have very different gut flora and enzymes.

      I'm just spit balling here, but we do know 2 things at least: The general population is still under the impression that calorie restriction is "good", and people still think they should avoid fat. So we have a perfect storm here of slowing down the thyroid (calorie restriction), and K2 deficiency (avoiding fat). You can still fix hypothyroidism by eating a ton of carbs w/ low fat, but that doesn't fix the possible K2 deficiency by avoiding fat.

      Now the problem trying to find studies on this, is one will always find conflicting studies on whether HCLF causes CVD or HFLC causes CVD. But here is one from NCBI about dietary intake of K2 and it's effects on arterial calcification:

      The study is long I know, so I'll just highlight a couple of points in there:

      "Adequate intake of vitamin K2 has been shown to lower the risk of vascular damage because it activates MGP, which inhibits calcium from depositing in the vessel walls. Hence, calcium is available for multiple other roles in the body, leaving the arteries healthy and flexible"

      "However, vitamin K deficiency results in inadequate activation of MGP, which greatly impairs the process of calcium removal and increases the risk of calcification of the blood vessels"

      "The population-based Rotterdam study studied 4807 healthy men and women older than age 55 years, evaluating the relationship between dietary intake of vitamin K and aortic calcification, heart disease, and all-cause mortality.10 The study revealed that high dietary intake of vitamin K2—at least 32 mcg per day, with no intake of vitamin K1, was associated with a 50% reduction in death from cardiovascular issues related to arterial calcification and a 25% reduction in all-cause mortality."